Hayashi K, Chen W G, Chen Y Y, Murakami I, Chen H L, Ohara N, Nose S, Hamaya K, Matsui S, Bacchi M M, Bacchi C E, Chang K L, Weiss L M
Department of Pathology, City of Hope National Medical Center, Duarte, California 91010, USA.
Am J Pathol. 1998 Jan;152(1):191-8.
A 30-bp deletion in the Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) gene has been reported in nasopharyngeal carcinoma and EBV-associated malignant lymphomas. Information on this deletion in EBV-associated gastric carcinoma (EBVaGC) is limited. The association of gastric carcinoma (GC) with EBV was examined by EBV-encoded RNA (EBER) in situ hybridization in 510 patients from Japan and 80 patients from Brazil. We studied the prevalence of 30-bp LMP1 gene deletion in EBVaGC in Japan (29 cases) and Brazil (four cases) in comparison with the corresponding EBER1-positive metastatic lesions in lymph nodes (10 cases) and EBV-infected reactive lymphocytes from dissected nonmetastatic lymph nodes (22 cases), microdissected non-neoplastic gastric mucosa of EBVaGC (five cases), and EBV-nonassociated GC (25 cases). We studied the status of the LMP1 gene by Southern blot hybridization of polymerase chain reaction products obtained after amplification with primers flanking the site of the deletion. We also performed EBV typing and LMP1 protein immunohistochemistry. EBV DNA was amplified by polymerase chain reaction in 30 of 33 EBVaGC cases, 8 of 10 metastatic carcinomas, 14 non-neoplastic tissues from 27 EBVaGC cases, and 12 of 25 non-EBV-associated GC cases with EBER1-positive lymphocytes. The 30-bp LMP1 gene deletion was observed in 23 of 26 (88.5%) cases of EBVaGC from Japan and two of four (50%) cases of Brazilian EBVaGC as compared with EBER1-positive reactive lymphocytes from 11 of 14 (78.6%) EBVaGC cases and 9 of 12 (75%) cases of non-EBV-associated GC. The variant type (the 30-bp deletion variant or nondeleted wild type) of LMP1 gene was the same among reactive lymphocytes, primary and secondary lesions of EBVaGC in all cases for which all three tissue types were studied (six of six). There was no correlation between the presence of the 30-bp deletion with depth of cancer invasion or presence of metastasis. Type A was detected in all available EBV-positive cases. The similar high incidence of 30-bp deletion in LMP1 gene in both carcinoma cells and reactive lymphocytes in EBVaGC cases suggests that this deletion may not be relevant to the pathogenesis of EBVaGC.
据报道，在鼻咽癌和EB病毒（EBV）相关的恶性淋巴瘤中，EBV潜伏膜蛋白1（LMP1）基因存在30个碱基对的缺失。关于EBV相关胃癌（EBVaGC）中这种缺失的信息有限。通过EBV编码RNA（EBER）原位杂交技术，对来自日本的510例患者和来自巴西的80例患者的胃癌与EBV的相关性进行了检测。我们研究了日本（29例）和巴西（4例）EBVaGC中30个碱基对LMP1基因缺失的发生率，并与相应的EBER1阳性淋巴结转移灶（10例）、解剖的非转移淋巴结中的EBV感染反应性淋巴细胞（22例）、EBVaGC显微切割的非肿瘤性胃黏膜（5例）以及EBV非相关胃癌（25例）进行了比较。我们通过用缺失位点两侧的引物扩增后获得的聚合酶链反应产物进行Southern印迹杂交，研究了LMP1基因的状态。我们还进行了EBV分型和LMP1蛋白免疫组织化学检测。在33例EBVaGC病例中的30例、10例转移癌中的8例、27例EBVaGC病例的14个非肿瘤组织以及25例非EBV相关胃癌病例中EBER1阳性淋巴细胞的12例中，通过聚合酶链反应扩增了EBV DNA。与14例EBVaGC病例中的11例（78.6%）和12例非EBV相关胃癌病例中的9例（75%）的EBER1阳性反应性淋巴细胞相比，在日本26例EBVaGC病例中的23例（88.5%）和巴西4例EBVaGC病例中的2例（50%）中观察到了30个碱基对的LMP1基因缺失。在所有研究了三种组织类型的病例中，LMP1基因的变异型（30个碱基对缺失变异型或未缺失野生型）在反应性淋巴细胞、EBVaGC的原发和继发病变中是相同的（6例中的6例）。30个碱基对缺失的存在与癌症浸润深度或转移的存在之间没有相关性。在所有可用的EBV阳性病例中均检测到A型。EBVaGC病例中癌细胞和反应性淋巴细胞中LMP1基因30个碱基对缺失的相似高发生率表明，这种缺失可能与EBVaGC的发病机制无关。
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